Scientific workflows organize the assembly of specialized software into an overall data flow and are particularly well suited for multi-step analyses using different types of software tools. They are also favorable in terms of reusability, as previously designed workflows could be made publicly available through the myExperiment community and then used in other workflows. We here illustrate how scientific workflows and the Taverna workbench in particular can be used in bibliometrics. We discuss the specific capabilities of Taverna that makes this software a powerful tool in this field, such as automated data import via Web services, data extraction from XML by XPaths, and statistical analysis and visualization with R. The support of the latter is particularly relevant, as it allows integration of a number of recently developed R packages specifically for bibliometrics. Examples are used to illustrate the possibilities of Taverna in the fields of bibliometrics and scientometrics.

Mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 are found in a subset of benign and malignant cartilage tumors, gliomas and leukaemias. The mutant enzyme causes the production of D-2-hydroxyglutarate (D-2-HG), affecting CpG island and histone methylation. While mutations in IDH1/2 are early events in benign cartilage tumors, we evaluated whether these mutations play a role in malignant chondrosarcomas. Compared to IDH1/2 wildtype cell lines, chondrosarcoma cell lines harboring an endogenous IDH1 (n=3) or IDH2 mutation (n=2) showed up to a 100-fold increase in intracellular and extracellular D-2-HG levels. Specific inhibition of mutant IDH1 using AGI-5198 decreased levels of D-2-HG in a dose dependent manner. After 72 hours of treatment one out of three mutant IDH1 cell lines showed a moderate decrease in viability, while D-2-HG levels decreased >90%. Likewise, prolonged treatment (up to 20 passages) did not affect proliferation and migration. Furthermore, global gene expression, CpG island methylation as well as histone H3K4, -9, and -27 trimethylation levels remained unchanged. Thus, while IDH1/2 mutations cause enchondroma, malignant progression towards central chondrosarcoma renders chondrosarcoma growth independent of these mutations. Thus, monotherapy based on inhibition of mutant IDH1 appears insufficient for treatment of inoperable or metastasized chondrosarcoma patients.

In this study, we assess the effects of temporary employment on job satisfaction and the personal lives of recent PhD graduates. Temporary employment is becoming increasingly prevalent in many sectors, but has been relatively common in academia, especially for early career scientists. Labor market theory shows temporary employment to have a conspicuous negative influence on the job satisfaction and well-being of employees, but also identifies groups that may be exempt from these negative influences, such as the highly educated. Here, we study the effect of temporary employment on the highest educated group in the labor force, PhD graduates. We present findings of a survey of 1133 respondents who obtained their PhD from one of five Dutch universities between 2008 and 2012. Compared to PhDs employed on a permanent contract, PhDs on a temporary contract are less satisfied with their terms of employment, especially if they have no prospect of permanence. Temporary contracts with no prospect of permanence also decrease satisfaction with job content. Conversely, self-employment increases satisfaction with job content. Educational level required for the job also influences job satisfaction to a large degree: working below PhD level negatively affects job satisfaction. Finally, the type of contract affects different aspects of the personal lives of PhDs, such as the ability to obtain a mortgage, the stability of family life, and the possibility to start a family. In conclusion, we show that the highest educated, i.e., PhD graduates are not exempt from the negative influences of temporary employment.Electronic supplementary material The online version of this article

Multiple osteochondromas (MO) is an autosomal dominant disorder caused by germline mutations in EXT1 and/or EXT2. In contrast, solitary osteochondroma (SO) is nonhereditary. Products of the EXT gene are involved in heparan sulfate (HS) biosynthesis. In this study, we investigated whether osteochondromas arise via either loss of heterozygosity (2 hits) or haploinsufficiency. An in vitro three-dimensional chondrogenic pellet model was used to compare heterozygous bone marrow-derived mesenchymal stem cells (MSCs EXT(wt/-)) of MO patients with normal MSCs and the corresponding tumor specimens (presumed EXT(-/-)). We demonstrated a second hit in EXT in five of eight osteochondromas. HS chain length and structure, in vitro chondrogenesis, and EXT expression levels were identical in both EXT(wt/-) and normal MSCs. Immunohistochemistry for HS, HS proteoglycans, and HS-dependent signaling pathways (eg, TGF-β/BMP, Wnt, and PTHLH) also showed no differences. The cartilaginous cap of osteochondroma contained a mixture of HS-positive and HS-negative cells. Because a heterozygous EXT mutation does not affect chondrogenesis, EXT, HS, or downstream signaling pathways in MSCs, our results refute the haploinsufficiency theory. We found a second hit in 63% of analyzed osteochondromas, supporting the hypothesis that osteochondromas arise via loss of heterozygosity. The detection of the second hit may depend on the ratio of HS-positive (normal) versus HS-negative (mutated) cells in the cartilaginous cap of the osteochondroma.

IntroductionThe medical field is currently facing a physician-scientist shortage. One possible solution is to direct medical students towards a research oriented career. To do so, knowledge is needed on how to motivate medical students to do research. Therefore, this study examines motivation for research and identifies factors influencing intrinsic and extrinsic motivation for research among first-year medical students.MethodsFirst-year medical students were surveyed at the beginning of their bachelor’s program in 2016. On a 7-point Likert scale, students reported their motivation for research, self-efficacy, perceptions of research, curiosity, and need for challenge. Regression analyses were used to examine the influence of these factors on students’ motivation for research.ResultsOut of 316 approached students, 315 participated (99.7%). On average, students scored 5.49 on intrinsic, and 5.66 on extrinsic motivation for research. All factors measured influenced intrinsic and extrinsic motivation for research significantly and positively, also after adjusting for gender and age. Cumulative regression showed that these factors explained 39.6% of the variance in intrinsic, and 14% in extrinsic motivation for research.DiscussionAll factors play an important role in intrinsic and, to a lesser extent, extrinsic motivation for research. First-year medical students’ motivation for research could be enhanced by stimulating positive self-efficacy beliefs, positive perceptions of research, and curiosity. Also, it is important to fulfil students’ needs for challenge by stimulating them to actively conduct research. Thus, to catch students young and cultivate physician-scientists, students should be stimulated to engage in research from the beginning of medical training.